Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

• Published in: Bioengineered 2022-03, Vol.13 (3), p.7880-7892
• Main Authors: Gao, Xin, Fan, Xinlong, Zeng, Wei, Liang, Jiwang, Guo, Nan, Yang, Xiao, Zhao, Yuejiao
• Format: Article
• Language: English
• Subjects: Apoptosis - genetics; cell behavior; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Head and Neck Neoplasms; Humans; Hypopharyngeal squamous cell carcinoma; MicroRNAs - genetics; MicroRNAs - metabolism; miR-107; NOB1; Nuclear Proteins - metabolism; Phosphatidylinositol 3-Kinase - metabolism; Phosphatidylinositol 3-Kinases - genetics; Phosphatidylinositol 3-Kinases - metabolism; PI3K/Akt; Proto-Oncogene Proteins c-akt - genetics; Proto-Oncogene Proteins c-akt - metabolism; Research Paper; RNA-Binding Proteins - metabolism; Signal Transduction - genetics; Squamous Cell Carcinoma of Head and Neck
• ISSN: 2165-5979; 2165-5987
• DOI: 10.1080/21655979.2022.2051266

Hypopharyngeal squamous cell carcinoma (HSCC) is one of the most common head and neck cancers, with a worst prognosis owing to its aggressivity. MicroRNA-107 (miR-107) is reported to regulate the progression of various cancers. Nevertheless, its implied function in HSCC remains unclear. This study is aimed to exploring the roles and potential mechanisms of miR-107 in HSCC. We found that miR-107 expression was significantly decreased in HSCC tissues compared with the para-cancer tissues. Moreover, miR-107 overexpression by miR-107 mimics decreased FaDu cell viability, led to cell cycle arrest in G1/S phase, accelerated apoptosis, and reduced cell migration and invasion. MiR-107 possibly resulted in deactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, evidenced by the decrease of phosphorylated (p-) PI3K and p-Akt. Besides, dual-luciferase reporter assay confirmed that miR-107 might bind to the 3'UTR of Nin one binding protein 1 (NOB1), and elevated NOB1 expression in HSCC tissues and a negative correlation between miR-107 and NOB1 were found. Rescue assays demonstrated the significant roles of miR-107 in FaDu cell behavior by modulating NOB1. In addition, the tumorigenic potential of miR-107 in vivo was conducted. It was found that miR-107 overexpression in FaDu cells significantly inhibited tumor growth and led to inactivation of the PI3K/Akt signaling. The above findings revealed that miR-107 could suppress FaDu cell proliferation, migration, invasion and induced apoptosis by targeting NOB1 through the PI3K/Akt pathway, suggesting that miR-107/NOB1 axis may exert a key role in FaDu HSCC development.